Specific neuronal subpopulations in the rat basolateral amygdala express high levels of nonphosphorylated neurofilaments.

Specific neuronal subpopulations in the rat basolateral amygdala express high levels of nonphosphorylated neurofilaments.
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大鼠基底外侧杏仁核中的特定神经元亚群表达高水平的非磷酸化神经丝。

DOI:
10.1002/cne.25169
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发表时间:
2021-09
期刊:
The Journal of comparative neurology
影响因子:
--
通讯作者:
Mascagni F
Mascagni F
中科院分区:
其他
文献类型:
--
作者:
McDonald AJ;Mascagni F

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含有非磷酸化神经丝(NNF)的皮质锥体神经元(PN)被SMI-32单克隆抗体定位,已被证明在阿尔茨海默病(AD)中特别容易变性。本研究首次研究了SMI-32+ NNF在杏仁核基底外侧核复合体(BNC)神经元中的表达,该复合体包含皮质样PNs和非锥体神经元(NPNs)。我们观察到,在大鼠基底外侧核(BL),但不是在外侧(LAT)或基底内侧(BM)核的PN,具有显着水平的SMI-32-ir在其胞体与抗体稀释液,不含Triton X-100,但染色在这些细胞大大减弱时,抗体稀释液含有0.3%的Triton。使用含Triton的稀释剂,我们发现所有三个BNC核中的所有SMI-32+神经元都是NPN。使用双标记免疫过氧化物酶技术,我们证明了这些SMI-32+ NPN中的大多数是小清蛋白阳性(PV+)或生长抑素阳性的NPN,但不是血管活性肠肽阳性或神经肽Y阳性的NPN。使用一种技术,结合逆行追踪与SMI-32免疫组织化学使用中间水平的Triton的稀释剂,我们发现,所有的BNC神经元投射到丘脑背内侧核(MD)的大NPN,和大多数是SMI-32+。相反,投射到腹侧纹状体或大脑皮质的BNC神经元是在BL中表达低水平SMI-32免疫反应性(SMI-32-ir)的PN,而在LAT或BM中没有SMI-32-ir。这些数据表明,主要的神经元亚群在BNC退化的AD可能是PV+和MD投射的NPN。
Cortical pyramidal neurons (PNs) containing non-phosphorylated neurofilaments (NNFs) localized with the SMI-32 monoclonal antibody have been shown to be especially vulnerable to degeneration in Alzheimer’s disease (AD). The present investigation is the first to study the expression of SMI-32+ NNFs in neurons of the basolateral nuclear complex of the amygdala (BNC), which contains cortex-like PNs and nonpyramidal neurons (NPNs). We observed that PNs in the rat basolateral nucleus (BL), but not in the lateral (LAT) or basomedial (BM) nuclei, have significant levels of SMI-32-ir in their somata with antibody diluents that did not contain Triton X-100, but staining in these cells was greatly attenuated when the antibody diluent contained 0.3% Triton. Using Triton-containing diluents we found that all SMI-32+ neurons in all three of the BNC nuclei were NPNs. Using a dual-labeling immunoperoxidase technique we demonstrated that most of these SMI-32+ NPNs were parvalbumin-positive (PV+) or somatostatin-positive NPNs, but not vasoactive intestinal peptide-positive or neuropeptide Y-positive NPNs. Using a technique that combines retrograde tracing with SMI-32 immunohistochemistry using intermediate levels of Triton in the diluent we found that all BNC neurons projecting to the mediodorsal thalamic nucleus (MD) were large NPNs, and most were SMI-32+. In contrast, BNC neurons projecting to the ventral striatum or cerebral cortex were PNs that expressed low levels of SMI-32 immunoreactivity (SMI-32-ir) in the BL, and no SMI-32-ir in the LAT or BM. These data suggest that the main neuronal subpopulations in the BNC that degenerate in AD may be PV+ and MD-projecting NPNs.
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